Management of Hypertension in

Hemodialysis Patients
C. Venkata S. Ram, MD, and Andrew Z. Fenves, MD

Corresponding author
C. Venkata S. Ram, MD
1420 Viceroy Drive, Dallas, TX 75235, USA.
E-mail: ramv@dneph.com
Current Hypertension Reports 2009, 11:292298
Current Medicine Group LLC ISSN 1522-6417
Copyright 2009 by Current Medicine Group LLC

Hypertension is very common in patients with

chronic kidney disease and is present in most patients
with end-stage renal disease (ESRD). Hypertension
is largely responsible for premature cardiovascular
disease in dialysis patients. The pathophysiology
of hypertension in ESRD is complex, and multiple
mechanisms are likely involved in blood pressure dysregulation in patients on hemodialysis. Some of these
patients demonstrate resistant hypertension. Aggressive control of hypertension in ESRD/dialysis is
mandatory. Generally, nonpharmacologic treatments
are not enough to achieve the goal blood pressure
levels in dialysis patients. Multiple antihypertensive
drugs are often necessary. Drugs that block the reninangiotensin system offer a number of advantages for
patients with chronic kidney disease or ESRD, but
additional drug classes are often needed to achieve
effective blood pressure control in dialysis patients.
Physicians treating hypertension in dialysis patients
should be familiar with the pharmacokinetic properties of antihypertensive drugs in renal failure and
choose the dosages accordingly. Vigorous control of
hypertension is recommended to reduce the disease
burden in patients with ESRD.

Introduction
Systemic hypertension in patients undergoing chronic
dialysis presents a major therapeutic challenge in clinical
medicine. Because it is a cause as well as a consequence of
chronic kidney disease (CKD) and end-stage renal disease
(ESRD), hypertension not only is prevalent in patients
undergoing dialysis but also is a critical contributor to
excessive cardiovascular morbidity and mortality in these
high-risk patients. Hypertension occurs in more than 80%
of patients who have ESRD [1]. The prevalence and degree
of hypertension is steadily increasing in patients undergoing hemodialysis or chronic ambulatory peritoneal dialysis.

Despite advances in the physiology and pharmacology of

blood pressure control mechanisms, hypertension remains
poorly controlled in patients with ESRD (Table 1). Uncontrolled hypertension contributes to excessive cardiovascular
morbidity and mortality in dialysis patients.
Systemic hypertension is a risk factor for vascular disease,
accelerated progression of atherosclerosis, left ventricular
hypertrophy, and cardiac dysfunction. Cardiovascular disease accounts for the high mortality rate in patients with
ESRD, and hypertension is the most powerful link to cardiovascular disease in this population [2]. The presence of other
risk factors for cardiovascular disease, such as diabetes and
hyperlipidemia, imposes further risk in patients with ESRD.

Pathophysiologic Factors
The etiology of hypertension in ESRD is complex and
multifactorial. With the establishment and progression of
hypertension in ESRD, the hemodynamic milieu changes
dramatically with complicated interactions among the
mechanisms of circulatory control. Because of the complex
interplay of various pathophysiologic processes, treatment
of hypertension in ESRD is extremely difficult and the
therapeutic response is often unpredictable. In a substantial number of patients on dialysis, removal of excess fluid
and achievement of dry weight improves blood pressure
control. Patients with ESRD demonstrate a rise in cardiac
output as a reaction to anemia. In normotensive patients
with ESRD, the rise in cardiac output is accompanied by
a fall in peripheral vascular resistance; in hypertensive
patients, however, this reciprocal adaptive change fails to
occur, culminating in a blood pressure rise. The discussion in this article applies to hemodialysis patients but
not to peritoneal dialysis patients, with some exceptions.
Blood pressure control in patients undergoing peritoneal
dialysis is less difficult than in hemodialysis patients.

Extracellular fluid volume expansion

The volume of extracellular fluid (ECF) is probably the
most important determinant of hypertension in ESRD
patients [37]. ECF expansion is not always accompanied
by detectable edema. ECF volume retention leads to an
increase in cardiac output against the setting of inappropriate systemic vascular resistance, with the ultimate result
of rising blood pressure. This hemodynamic imbalance
is further complicated by the failure to inhibit vasocon-

Management of Hypertension in Hemodialysis Patients

Table 1. Reasons for lack of control of

hypertension in dialysis patients
Staff satisfaction with level of blood pressure
Insufcient attention to lifestyle modication
Patient noncompliance with salt and uid intake
Inadequate ultraltration
Inadequate prescription of medications
Underlying secondary form of hypertension

strictor mechanisms such as the renin angiotensin system

(RAS) and sympathetic nervous system (SNS) [8,9]. The
ultrafi ltration component of dialysis improves the blood
pressure in ESRD (at times, rather dramatically), reflecting the volume-dependent factor in these patients. In
some patients, however, it may take frequent dialysis to
produce an improvement in blood pressure. Hence, even
in so-called volume-dependent hypertension, removal of
ECF alone may not explain the blood pressure dynamics
in ESRD. Nevertheless, achievement and maintenance
of dry weight is a crucial component of hypertension
management in ESRD. Inadequate removal of ECF volume is major cause of resistant hypertension in dialysis
patents. Dry weight is not a fi xed measure and is variable.
It is impossible to keep the patient dry constantly; the
idea is to prevent volume overload as a pathogenetic factor for persistent hypertension. ECF overload in ESRD is
due to the loss of renal excretory function and the absence
of vasodilatory renoprival factors such as prostaglandins.
Because not only the volume factor but also the activity
of vasoconstrictor forces such as RAS and SNS mediate
blood pressure homeostasis, inappropriate activity of SNS
and RAS (high or even normal) in the context of volume
overload clearly contributes to the onset and development
of hypertension in ESRD patients on dialysis.
The role of the RAS pathway in the genesis of ESRD
hypertension is evident from the effectiveness of bilateral
nephrectomy, which instantly removes the main source of
renin in dialysis patients. There is an inverse correlation
between systemic vascular resistance and Na+/K+ adenosine triphosphatase (ATPase) activity. In dialysis patients,
there is increased secretion of ouabain-like inhibitors
of Na+/K+ ATPase activity. When the actions of Na+/K+
ATPase are inhibited in the vascular smooth muscle,
the intracellular Na+ level and the cytosolic Ca+2 level
increase, leading to significant vasoconstriction. Regardless of the mechanism of vasoconstriction, removal of
ECF volume and attainment of dry weight often improve
blood pressure control in dialysis patients. It is worth
remembering that the degree of volume overload is classically reflected by an increase in blood pressure rather
than by the appearance of frank edema. It is important
to emphasize to patients that the therapeutic gains from
dialysis can be sustained only if salt intake is curtailed
between dialysis sessions.

Ram and Fenves

293

Renin-angiotensin system activation

The role of the RAS in the etiology of hypertension in
ESRD is well established [8,9]. In hemodialysis patients
with ESRD, there is an abnormal relationship between
blood volume, exchangeable sodium, and plasma renin
activity. Bilateral nephrectomy improves blood pressure
control in dialysis patients with severe hypertension, presumably by removing the basic biologic source of renin.
Indirect evidence for the participation of the RAS in
hypertension associated with ESRD is the prompt therapeutic response seen with the use of drugs that block the
RAS. It is also possible that aldosterone may play a role in
the genesis of hypertension in dialysis patients. Failure to
suppress the RAS despite volume expansion identifies this
mechanism as a principal mediator of vasoconstriction
and blood pressure elevation in patients on dialysis.

Sympathetic nervous system activity

It is well known that uremia and ESRD are associated
with enhanced SNS activity [1012]; measurement of
peroneal nerve activity in ESRD has confi rmed the role
of SNS activation in this setting [13]. The afferent signal
for SNS activity most likely resides in the kidney itself,
as the nerve activity is diminished in the anephric state.
Although plasma concentrations of catecholamines are
elevated in ESRD, this fi nding must be interpreted with
caution because of altered metabolism and kinetics of
epinephrine and norepinephrine in CKD. The increase
of SNS activity is triggered by an excitatory signal
arising in the failing kidney; uremia stimulates chemosensitive afferent nerves in the kidney. Selective surgical
removal of affected renal nerves prevents hypertension
in experimental renal injury. Hemodialysis patients with
bilateral nephrectomy show the same level of sympathetic discharge as normal controls. Another possible
neurogenic mechanism in anemic patients is reduced
central dopaminergic tone. In chronic renal failure, the
biologic actions of dopamine are attenuated, resulting
in a reflexive increase in SNS activity. Abnormal vagal
tone and reduced baroreceptor sensitivity have also been
implicated as mechanisms of hypertension in ESRD that
involve SNS activation.

Erythropoietin use
Therapeutic application of recombinant human erythropoietin (rHuEPO) has been a significant advance in the
management of anemia in ESRD/hemodialysis patients.
Unfortunately, rHuEPO increases blood pressure by
causing vasoconstriction and increasing the blood viscosity (Table 2) [1416]; correction of anemia also prevents
hypoxia-mediated vasodilatation. The rise in blood pressure with the use of rHuEPO occurs within 2 to 12 weeks
of therapy. Rapid correction of anemia and a prior history of hypertension are important predisposing factors.
Both anemia and its overcorrection can be detrimental, so
every attempt should be made to keep the maximum level
of hemoglobin between 10 and 12 g/dL.

294

The Therapeutic Trials

Table 2. Factors in the pathogenesis of

hypertension in ESRD patients on erythropoietin
Increased blood viscosity
Increased blood volume
Increased total peripheral resistance
Loss of hypoxic vasodilation
Enhanced sensitivity to circulating
catecholamines and angiotensin II
Direct vasoconstrictor effect
Increased cytosolic calcium
Stimulation of endothelin
ESRDend-stage renal disease.

The risk of hypertension is higher in patients receiving

rHuEPO intravenously rather than subcutaneously, and
the degree of hypertension is dose-dependent. Treatment
with rHuEPO increases blood viscosity, blood volume,
plasma endothelin, and catecholamines, and it may also
cause direct vasoconstriction. The benefits of rHuEPO
in correcting anemia outweigh the risk of hypertension,
however, as the hypertension can be controlled by dialysis
and antihypertensive drugs. The dosage of rHuEPO can
be reduced with the use of adjunct therapies such as iron,
thus minimizing the risk of hypertension.

dialysis-associated hypertension [21,22]. The extent

to which an NO defect contributes to hypertension in
chronic renal failure is not fi rmly established. An endogenous inhibitor of NO, asymmetric dimethylarginine,
accumulates in ESRD and thus may predispose to hypertension. Increased function of the SNS also may inhibit
NO availability.
An endothelium-derived vasoconstricting factor,
endothelin-1 (ET-1), is expressed in the blood vessels.
ET-1 promotes vasoconstriction and fi brosis. It has
been suggested that hypertensive ESRD patients have
higher levels of ET-1 than normotensive patients. It is
of interest to note that ET-1 levels are more affected
in hemodialysis patients than in peritoneal dialysis
patients. Whether directly or indirectly, ET-1 may
be abnormally regulated in hypertensive patients on
dialysis [23,24].

Prostaglandins
Because renal prostaglandins and prostacyclin cause
vasodilatation, a deficiency of these mediators in ESRD
may increase blood pressure. They also offset vasoconstrictor influences. Hence, renal prostaglandins may play
a pathologic role in blood pressure regulation in patients
with ESRD.

Treatment of Hypertension
Divalent ions and parathyroid hormone
Intracellular levels of calcium are increased in patients
with chronic renal failure, and there is a direct pathophysiologic correlation between intracellular calcium and
blood pressure levels in dialysis patients with hypertension. Studies have shown a positive correlation between
intracellular and platelet calcium, serum parathyroid
hormone (PTH), and blood pressure levels in patients
with chronic renal failure [1719]. Hypercalcemia is more
likely to raise blood pressure in the presence of increased
PTH levels because of vasoconstriction, not cardiac output changes. Exogenous use of vitamin D analogues and
oral calcium supplementation are some factors contributing to hypercalcemia in ESRD. Augmentation of RAS and
SNS activity may also raise cytosolic concentrations of
calcium. Correction of hyperparathyroidism by vitamin
D administration or parathyroidectomy may lower blood
pressure in patients with ESRD. PTH appears to play a
role in the development of hypertension associated with
hypercalcemia in ESRD.

Endothelial factors
The role of endothelial cells in regulating vasomotor tone
and systemic vascular resistance is well established. The
availability and actions of endothelium-derived relaxation
factornow identified as nitric oxide (NO)governs the
state of vasoactive tone [20]. An absolute or relative deficiency of NO leads to a rise in the blood pressure level.
This mechanism may play a role in the development of

Treating hypertension in the dialysis patient can be

diffi cult, and a number of hemodynamic and pharmacologic factors must be considered. As in the management
of general hypertension, nonpharmacologic approaches
should be attempted fi rst, before resorting to drug
therapy [25,26]. Lifestyle modifi cation and hygienic
measures to maintain cardiovascular health should be
implemented. If these measures fail or are inadequate,
appropriate antihypertensive drugs should be chosen
for the dialysis patient. Achievement and maintenance
of optimal dry weight through appropriate sodium and
fluid restriction and dialysis frequency is a critical step
for blood pressure control [27]. After initiating dialysis, dry weight should be accomplished over a period
of 6 to 8 weeks, keeping in mind that the negative fluid
balance should not exceed 1 to 2 kg per week. Excessive ultrafi ltration may result in hypoperfusion and
ischemia. It is impossible to defi ne dry weight precisely,
but in clinical terms, dry weight can be characterized as
the body weight at the end of dialysis below which further ultrafi ltration causes hypotension. Estimation of
dry weight is a practical problem; several methods have
been proposed but none are feasible in clinical practice.
Nevertheless, fluid balance is of clinical importance in
the dialysis patient [2830]. Although aggressive ultrafi ltration is sometimes indicated (for congestive heart
failure, complicated hypertension, etc.), overzealous
dialysis may result in paradoxical hypertension because
of activation of the RAS and SNS.

Management of Hypertension in Hemodialysis Patients

Unless hypertension is severe, antihypertensive drug

therapy need not be instituted until dry weight is achieved.
In patients taking antihypertensive drugs, the doses can
be reduced while dry weight is achieved through dialysis.
For many patients, dry weight alone is enough to achieve
goal blood pressure. The problem is that the blood pressure often goes up in the interdialytic periods. Judicious
use of antihypertensive drugs is indicated to manage interdialytic hypertension. Carefully monitored ultrafi ltration
is the most important determinant of effective blood
pressure control in the dialysis patient. Because of the difficulty of estimating dry weight, nephrologists must apply
their judgment and clinical experience. It is important for
patients to maintain a high level of nutrition to complement the benefits of hemodialysis.
When the blood pressure cannot be controlled with
proper ultrafi ltration alone, antihypertensive drugs
should be used in dialysis patients. In general, except for
diuretics, the pharmacologic options for dialysis patients
do not differ very much from those used to treat primary
hypertension. From a pathophysiologic standpoint, drugs
that block the RAS are desirable to treat hypertension in
the dialysis patient, but in our experience, this approach
alone is not enough; multiple drugs are often necessary.
Physicians should be cognizant of the altered pharmacokinetics of antihypertensive drugs in renal failure and
should choose drugs and dosages accordingly.

Renin-angiotensin system blockers

Because several factors mediating hemodynamic variables
in ESRD are governed by the activity of the RAS, pharmacologic approaches to block this system are widely
applied to treat hypertension in dialysis patients [3133].
Interruption of the RAS with angiotensin-converting
enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) reduces systemic vascular resistance without
affecting cardiac output. RAS blockers have been shown
to be not only effective but also advantageous in patients
with CKD, but whether the same observation can be
translated to ESRD has not been proven. Effective inhibition of the RAS along with dialysis causes regression of
left ventricular hypertrophy.
ACE inhibitors
ACE inhibitors may decrease the circulating levels of
angiotensin (and aldosterone) and thus offset the vasoconstrictor consequences of inappropriate RAS activation
in patients with ESRD. An advantage of ACE inhibitors
(in contrast to direct vasodilators) is inhibition of the
counter-regulatory compensatory systems like the SNS.
Hence, the fall in blood pressure, if achieved, is likely to be
maintained with continued ACE inhibitor therapy. Moreover, ACE inhibitors improve (or do not worsen) insulin
sensitivity, a benefit in patients with coexisting diabetes.
Most patients on dialysis require multiple antihypertensive drugs, one of which should be an RAS blocker if there
are no contraindications or adverse effects.

Ram and Fenves

295

ACE inhibitors are generally well tolerated. Possible

adverse effects include cough, angioedema, rash, and
(rarely) leukopenia. A notable side effect of ACE inhibitors
is the worsening of anemia in dialysis patients; aggravation of anemia by ACE inhibitors in CKD is unpredictable
(or may be unrecognized) because of its chronic, insidious
nature and other contributing factors to anemia development in ESRD. Inhibition of angiotensin II activity may
block signal transduction of erythropoietin at the cellular level. Anaphylactic reactions have been reported with
ACE inhibitors in ESRD patients undergoing dialysis with
a high-flux capillary dialyzer.
Angiotensin receptor blockers
ARBs pharmacologically block the effects of angiotensin
II on the blood vessels and other tissues. The dominant
mechanism of ARBs in the treatment of hypertension is the
inhibition of angiotensin IImediated vasoconstriction;
to some extent, they also modulate SNS tone indirectly.
ARBs are extremely useful in patients with CKD, especially those with diabetic nephropathy and proteinuric
disorders [3436]. However, whether these fi ndings can
be extrapolated to patients with ESRD is not established.
Nevertheless, like ACE inhibitors, ARBs also exert a number of hemodynamic and nonhemodynamic advantages
in managing hypertension associated with ESRD. Unlike
ACE inhibitors, however, ARBs are unlikely to cause
cough, rash, or angioedema, and anaphylactic reactions
to ARBs are also rare in patients undergoing dialysis with
a high-flux capillary dialyzer.

Calcium channel blockers

Intracellular calcium exerts a number of actions on
blood pressure control mechanisms by its effects on vascular smooth muscle and other pressor systems (SNS,
RAS, etc.). Calcium channel blockers (CCBs) block the
voltage-dependent calcium channels, thereby inhibiting
vascular smooth muscle activity. Because of their proven
antihypertensive properties, CCBs are widely used in
patients on hemodialysis [3739]. The dihydropyridine
(DHP) subclass of CCBs (nifedipine, amlodipine, and
felodipine) are more effective than non-DHP CCBs
(eg, verapamil, diltiazem). Because CCBs have a greater
antihypertensive effect in the volume-expanded state,
these drugs are particularly suitable for ESRD patients.
Importantly, the pharmacokinetics of CCBs are not
altered in ESRD, so the dosages do not require any
modification. In the United States Renal Data System
dataset, the use of CCBs was associated with a lower risk
of cardiovascular morbidity and mortality [40]. Because
of their powerful antihypertensive properties and favorable cardiovascular protection, CCBs are used widely in
the treatment of hypertension in dialysis patients. CCBs
(either as monotherapy or as a component of combination
therapy) are generally well tolerated by dialysis patients.
DHP CCBs may cause tachycardia or headache, which
often resolves with continued treatment. Unless there are

296

The Therapeutic Trials

no other available options, sublingual nifedipine should

not be used because of the risk of inducing precipitous
hypotension. DHP CCBs can be safely given along with
other classes of antihypertensive drugs, including blockers. Non-DHP CCBs may cause heart block and
decreased output in susceptible patients; they should be
used with considerable caution, if at all, with -blockers because of the potential for synergistic myocardial
depression. Non-DHP CCBs, however, are preferred
over DHP CCBs in patients with supraventricular tachycardia, angina, or both.

-Adrenergic blocking drugs

-Blockers remain an important choice in the selection
of drugs for hypertension management, including drugs
for patients with ESRD. In the past, -blockers were
a popular component of triple drug therapy (vasodilator, -blocker, and a diuretic) for hypertension in CKD.
Because of their favorable outcomes in reducing cardiovascular mortality and morbidity, -blockers are useful
in the treatment of hypertension in patients with ESRD.
Because of the high prevalence of coronary artery disease
and congestive heart failure in the hemodialysis population, there is a sound rationale for the use of -blockers
in patients with ESRD. Renin suppression by -blockers
is another desirable pharmacologic property of immense
importance in patients with CKD/ESRD. A number of
-blockers have pharmacologic properties (eg, lipid solubility, cardioselectivity) that make them a helpful choice
for hypertension treatment in CKD/ESRD. It is unusual
for -blockers alone to control hypertension in hemodialysis patients, but they are often a necessary component
of multidrug therapy. In addition to the usual contraindications, clinicians should consider possible adverse effects
such as depression, erectile dysfunction, fatigue, and lipid
or glucose abnormalities.

-Adrenergic blocking drugs

-Blockers such as prazosin, terazosin, and doxazosin
have a diminishing role in the modern management of
hypertension; often, they are considered as add-on
drugs. Because of the availability of better-tolerated and
more effective antihypertensive drugs, the use of -blockers has decreased substantially. There are no prospective
outcome studies with -blockers in the CKD population,
and they offer no special advantages. In patients with
resistant hypertension, if an -blocker is used, effects
such as postural hypotension should be monitored. No
dose adjustment is needed in patients with CKD/ESRD.

Dual inhibitors of and receptors

Adrenergic inhibition can be achieved with dual inhibitors of and receptors, using drugs such as labetalol
and carvedilol. These drugs have not been systematically evaluated in patients with CKD/ESRD. Carvedilol
has been shown to have advantageous effects on glucose and lipid metabolism in hypertension, but it is

not known whether these fi ndings can be extended to

patients with CKD/ESRD.

Centrally acting sympathetic agonists

The central nervous system sympathetic agonists such as
clonidine, guanabenz, and methyldopa are used less frequently in current treatment strategies for hypertension
control. They are not popular because of effects such as
dry mouth, erectile dysfunction, fatigue, and rebound
hypertension. Clonidine requires downward dose adjustment in patients with ESRD. Clonidine has been found
to be useful in treating restless legs syndrome in chronic
dialysis patients. Like other sympathetic inhibiting drugs,
clonidine is considered as an add-on (not a primary)
option to treat hypertension in ESRD patients. Because
of their high side-effect profile, sympathetic inhibitors
(reserpine, guanethidine) are rarely used to treat hypertension in the ESRD population.

Direct vasodilators
Despite the advent of effective dialysis and modern
antihypertensive drugs, some patients with ESRD have
a therapeutic need for old direct vasodilators such as
hydralazine and minoxidil to achieve their goal blood
pressure levels. Before the availability of RAS blockers
and CCBs, direct vasodilators were used extensively in
ESRD to control hypertension: both hydralazine and minoxidil, in conjunction with adequate volume control and
-blockade, lowered the blood pressure significantly.
Because of brisk stimulation of reflex SNS activity,
direct vasodilator therapy should be accompanied by
simultaneous -blockade to offset tachycardia. To minimize adverse effects, the total daily dose of hydralazine
should not exceed 200 mg. For all practical purposes,
minoxidil can be considered a more potent version of
hydralazine. It is a powerful vasodilator and is advocated for severe and resistant forms of hypertension. The
adverse-effect profi le of minoxidil is very similar to that
of hydralazine, with the addition of hair growth and
massive fluid retention (managed by ultrafi ltration). For
these reasons, the use of minoxidil is restricted. Despite
the complexities of using hydralazine and minoxidil, these
drugs have a practical role in the management of resistant
hypertension when they are used properly.

Secondary Hypertension
Secondary forms of hypertension should be considered
in the dialysis patient with resistant hypertension, based
upon clinical and laboratory parameters. Although
hypertension in patients with ESRD is generally
advanced and linked to the decline in renal function, a
secondary source (eg, renovascular or endocrine causes
or sleep apnea) should be pursued on clinical grounds
in selected patients. The extent of the workup should be
guided by the clinical course, patient characteristics, and
laboratory fi ndings.

Management of Hypertension in Hemodialysis Patients

Special Factors Affecting Blood Pressure

in ESRD
It is believed that long (and slow) ultrafi ltration may control hypertension more effectively in patients with ESRD.
The mechanism by which prolonged dialysis is helpful
is not understood; it may be mediated by the removal of
vasoconstrictor substances. Simply achieving dry weight
may not suffice for some patients on hemodialysis [41,42].
Some studies also suggest that nocturnal dialysis may
improve blood pressure control in hypertensive patients
with ESRD. Recent observations have indicated that
home blood pressure measurements may be highly useful in managing hypertension in hemodialysis patients,
and out-of-clinic blood pressure levels should be considered whenever possible in adjusting antihypertensive
drugs [43]. This modality deserves to be applied more
widely in the hemodialysis population, not only in ESRD
but also for all patients with CKD. Out-of-office blood
pressure measurements are superior to those in the dialysis clinic, and it is also known that intradialytic blood
pressure recordings are more sensitive and valuable than
predialytic/postdialytic blood pressure measurements in
managing hypertension [44].

Ram and Fenves

297

Control of hypertension in the dialysis patient requires

proper and efficient dialysis to maintain dry weight
and aggressive application of antihypertensive drugs.
Often multiple antihypertensive drugs are required. The
selection and dosages of these drugs depend on their
pharmacokinetics in ESRD and their dialyzability. With
judicious control of ECF volume and antihypertensive
drugs, combined with supervised, tightly monitored blood
pressure measurements, we can improve blood pressure
control rates in ESRD and thereby reduce the overall disease burden in this high-risk group of patients.

Acknowledgment
The authors thank Ms. Nanci Hassell for her assistance in
the preparation of this manuscript.

Disclosure
No potential confl icts of interest relevant to this article
were reported.

References and Recommended Reading

Conclusions
Systemic hypertension is extremely common in the ESRD
population, affecting a majority of patients undergoing
hemodialysis or peritoneal dialysis. Uncontrolled hypertension is a significant factor in premature cardiovascular
morbidity and mortality in this high-risk group. A number of hemodynamic and vasomotor mechanisms interact
in an adverse fashion to cause and maintain hypertension
in ESRD. Unless blood pressure is properly controlled,
ESRD patients are subject to various neurologic and
cardiovascular complications. Management of hypertension in the dialysis patient should take into consideration
variables such as lack of nocturnal fall in blood pressure
as well as interdialytic and ambulatory measurements of
blood pressure levels. Aggressive control of hypertension
is essential to decrease the progression of ESRD [45].
Although there is a controversy about whether excessive blood pressure control produces poor outcomes
in patients undergoing chronic ambulatory peritoneal
dialysis [46], no rigorously controlled clinical trials have
examined hypertension management in the dialysis population [47]. The points made in this article pertain mainly
to hemodialysis (the procedure used in the overwhelming
majority of ESRD patients in the United States) rather
than to peritoneal dialysis. In general, blood pressure control in peritoneal dialysis patients is superior to those on
hemodialysis. Hemodynamics in peritoneal dialysis are
more stable than in hemodialysis. The counter-regulatory
mechanisms such as RAS and SNS are less likely to be
activated by peritoneal dialysis than by hemodialysis, and
the clearance characteristics of peritoneal dialysis are distinctive and more physiologic than in hemodialysis.

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